Fasudil alleviates LPS-induced lung injury by restoring aquaporin 5 expression and inhibiting inflammation in lungs

摘要

Fasudil,a selective rho kinase (ROCK) inhibitor,has been reported to play a beneficial role in systemic inflammation in acute lung injury,but its mechanism for ameliorating pulmonary edema and inflammation remains unclear.Using hematoxylin-and-eosin (H&E) staining,immunohistochemistry,enzyme-linked immunosorbent assay,quantitative real time PCR and Western blotting,we found that fasudil attenuated LPS-induced lung injury,decreased lung edema,and suppressed inflammatory responses including leukocyte infiltration and IL-6 production.Further,fasudil upregulated LPS-induced aquaporin 5 reduction and inhibited NF-κB activation in the lungs of mice.Our results suggest that fasudil could restore the expression of aquaporin 5 to eliminate LPS-induced lung edema and prevent LPS-induced pulmonary inflammation by blocking the inflammatory pathway.Collectively,blockade of the ROCK pathway by fasudil may be a potential strategy for the treatment of acute lung injury.